Cerebellum - Tilmann-Braun Flashcards

1
Q

Anatomy and location of the cerebellum

A
  • very close to the brainstem
  • structure: several lobules (10) and fissures:
  • -> lobules are not all the same size (e.g. lobule 7 and 8 have multiple parts A,B..)
  • -> main fissure: primary fissure (dividing the anterior and posterior lobes)
  • Vermis: dividing the 2 hemispheres
  • hemisphere is subdivided into: paravermis (close to vermis) and lateral hemisphere
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2
Q

what are the 4 ways to subdivide the cerebellum?

A
  1. anatomy
  2. phylogenesis
  3. afferent
  4. efferent
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3
Q

according to the phylogenetic subdivision of the cerebellum, which part corresponds to the floculomodular lobe (anatomical subdivision)?

A

archicerebellum (the first part of the cerebellum to develop in evolution)

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4
Q

what are the afferent subdivisions of the cerebellum? what input does each part receive?

A
  • vestibulocerebellar - input from vestibular system (truncal ataxia, nystagmus)
  • pontocerebellum- input from the cortex through pons (asynergia, decomposition)
  • spinocerebellum - input from spinal cord (gait ataxia, dysarthria)
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5
Q

what are the efferent subdivisions of the cerebellum? what output does each part send?

A
  • medial zone- project to fastigial nucleus
  • intermediate zone - project to emboli form and globose
  • lateral zone - project to dentate nucleus
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6
Q

what is the function of each subdivision of the cerebellum?

A
  1. floculonodular lobe/ archicerebellum/ vestibulocerebellum/ festigial-vestibular nuclei:
    - eye movement, sitting, stance
  2. superior vermis- paravermal anterior lobe/ paleocerebellum/ spinocerebellum/ medial-intermediate zone (festigial and interpose nuclei):
    stance, gait, limb coordination
3. lateral hemisphere/ neocerebellum/ pontocerebellum/ dentate nucleus: 
limb coordination (planning), cognition
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7
Q

a patient has a tumour in the cerebellum, and shows symptoms of impaired balance and affected posture. which zone of the cerebellum is most likely affected?

a. intermediate zone
b. medial zone
c. lateral zone
d. lateral hemisphere

A

b. medial zone

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8
Q

what are the symptoms of ataxia of gait?

A
  • slow irregular step
  • short steps
  • increased stance phase
  • increased step width
  • feet rotated outward
  • variable joint rotation
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9
Q

what are the symptoms of limb ataxia?

A
  • dysmetria
  • intention tremor
  • asynergia
  • dysdiadochokinesis
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10
Q

what is asynergia?

A

decomposition of movements- it is compensation for complex movements, as patient avoids movements that involve multiple joints.

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11
Q

what is dysdiadocokinesis?

A

impaired sine when doing repetitive movements

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12
Q

cerebellar symptoms…

a. correspond to lesions located ipsilaterally (same side)
b. correspond to lesions located contalaterally (opposite side)
c. depending on the zone, the can corresoind to lesions located ipsi- or contralaterally

A

a

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13
Q

what are the symptoms of dysarthria?

A

slurred speech, scanning speech, high pitched speech,…

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14
Q

dysarthria is associated with lesions in lobule…

a. 1
b. 7
c. 8
d. 6
e. 3

A

d

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15
Q

what is ataxia?

A
  • ataxia is a disorder of the cerebellum, or its associated pathways.
  • poor coordination
  • many disorders of the cerebellum can cause ataxia (stroke, tumour…)
    exist in different forms - chronic, acute and subacute
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16
Q

which of the following statements about onset of ataxia is WRONG?

a. SCA is an autosomal dominant mutation that causes ataxia, onset usually starts in mid 20s
b. Friedrich’s ataxia is an autosomal recessive mutation, causes ataxia; onset >20 y
c. SAOA is a hereditary form of ataxia, onset starts at 30 y
d. MSA-C is a form of non-hereditary ataxia , onset starts around 50y
e. alcoholic cerebellar ataxia can occur at any age, since it is acquired during life.

A

c

–> onset of SAOA is >50y

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17
Q
T/F- 
Spinocerebellar ataxias (SCA) are a group of hereditary ataxias caused by a trinucleotide repeat
A

T

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18
Q

T/F-
SCA 1, 2 & 3 only have cerebellar symptoms ant therefore can be used as a model for studying cerebellar (dis-) functions, whereas SCA6 has also other symptoms that are not cerebellar

A

F

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19
Q

What are the signs of different SCAs?

A
  • SCA1- cerebellar signs + pyramidal tract signs
  • SCA2- cerebellar signs + slow saccades
  • SCA3- cerebellar signs + opthalomoplegia, pyramidal tract signs, dystonia
  • SCA6 - pure cerebellar
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20
Q

why isn’t Friedrich’s ataxia a good model for cerebellar ataxia?

A

FA starts in the DRG, spreads to the spinal cord and indirectly affects also cerebellar nuclei (dentate). It is not a purely cerebellar disease and most of its symptoms are not related to cerebellar dysfunction. In addition, due to its “non-cerebellar origin”, cerebellar lesions are not detected in scans. Thus it is not a good model for cerebellar ataxia

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21
Q

what are the symptoms of Friedrich’s ataxia?

A
  • macro square wave jerks
  • sensory ataxia
  • areflexia
  • pyramidal tract dysfunction
  • blindness & deafness
  • cardiomyopathy
  • sclerosis
  • diabetes type I and II
22
Q

atypical forms of Friedrich’s ataxia

A
  • late onset
  • very late onset
  • FA w. retained tendon reflexes
  • FA w. cerebellar atrophy
23
Q

T/F-
SAOA is an idiopathic cerebellar ataxia. It has purely cerebellar symptoms (like SCA6) and thus can be used as a model for cerebellar lesion.

A

T

24
Q

T/F-

MSA-C is a disease involving the cerebellum and brainstem

A

T

25
Q

which atrophy would you expect when looking at a MRI scan fron a patient with SCA1 ? is it a good cerebellar lesion model?

A

olivoponto-cerebellar atrophy (OPCA)

–> NOT a good cerebellar lesion model (not purely cerebellar)

26
Q

which atrophy would you expect when looking at a MRI scan fron a patient with SCA2 ? is it a good cerebellar lesion model?

A

olivoponto-cerebellar atrophy (OPCA)

–> NOT a good cerebellar lesion model (not purely cerebellar)

27
Q

which atrophy would you expect when looking at a MRI scan fron a patient with SCA3 ? is it a good cerebellar lesion model?

A

olivoponto-cerebellar atrophy (OPCA)

–> NOT a good cerebellar lesion model (not purely cerebellar)

28
Q

which atrophy would you expect when looking at a MRI scan fron a patient with SCA6 ? is it a good cerebellar lesion model?

A

cerebellar atrophy (CA) –> good cerebellar lesion model

29
Q

which atrophy would you expect when looking at a MRI scan fron a patient with Friedrich’s ataxia? is it a good cerebellar lesion model?

A

spinal atrophy –> NOT a good cerebellar lesion model

30
Q

which atrophy would you expect when looking at a MRI scan fron a patient with SAOA ? is it a good cerebellar lesion model?

A

cerebellar atrophy (CA) –> good cerebellar lesion model

31
Q

which atrophy would you expect when looking at a MRI scan fron a patient with MSA-C ? is it a good cerebellar lesion model?

A

olivoponto-cerebellar atrophy (OPCA) + hot cross bun sign

–> NOT a good cerebellar lesion model (not purely cerebellar)

32
Q

what would you expect to see in a MRI scan of an alcoholic patient?

A

cerebellar atrophy (mostly of the anterior lobe)

33
Q

what human cerebellar lesion models do you know?

A
  1. degenerative disorders- SCA6 and SAOA
  2. cerebellar strokes- SCA, PICA
  3. cerebellar tumours- astrocytoma
34
Q

what are the limitations of clinical rating scales of ataxia?

A

these scores are only based on observations, they are very subjective and require a lot of prior knowledge

35
Q

which of the following statements is/are correct?

a. the cerebellum acts as a timing device, a sensory analyser of sensory input, can predict, plan and execute movements and is important for learning and memory
b. the cerebellum is only important for motor control and functions.
c. the cerebellum model as a learning machine is an error based learning model
d. output from the cerebellum comes only from Purkinjee cells
e. the cerebellum is is important for pattern generation, for example in breathing

A

a, c, d

36
Q

how is information projected in the cerebellum? Why is the tidal wave equation a good model for timing in the cerebellum

A
  • When looking at the histology of the cerebellum, one can see that the only output going from the cerebellum comes from Purkinjee cells (PC).
  • input comes to PC –> PC inhibit cerebellar nuclei which are excitatory (modulatory fiction of PC).

Information projection in the cerebellum can be described as a tidal wave:

a. Afferents come from the pons and inferior olive through mossy fibres (MF) –> info goes to granular cells (GC)
b. GC send off axons which are split in ‘half’ and form T-shaped fibres.
c. there are many of these T-shaped fibres and they go in parallel to each other –> called parallel fibres (PF).
d. many PF excite the same PC at the same time, so the action is very well timed, and amplified, which allows PC to inhibit CN, so at the end very little output comes out of the cerebellum (because from PF it is all integrated simultaneously in PCs)

–> called tidal wave because a chain reaction generates a very well timed output

37
Q

what happens in cerebellar hypermetria?

A
  • in healthy subjects, movement of the limbs involves constriction of both the muscle and the opposite muscle.
  • in order to allow for a smooth movement, the muscle has to flex, and shortly after it stops, the opposite muscle has to constrict in order to enable movement of the limb.
  • in hypermetria, the muscle that has to flex, doesn’t peak as highly, and the flex lasts much longer. at the same time, the response from the opposite muscle comes way too late–> timing of the antagonist muscle is not properly done.
38
Q

which study has proven the role of the cerebellum as a sensory analyser?

A
  1. task I- the fingers of subjects were placed on sand paper
  2. task II- subjects felt sand paper of different graininess
  3. subjects had to decide which sand paper type has a finer graininess
    - -> there is a huge activation in the cerebellum when touching different surfaces–> activation rate varies depending on the surface
39
Q

how does the cerebellum predicts the error for motor control?

A

Error based learning:

  • The brain receives input fron the spinal cord and sensory input
  • Input is projected back and forth through the brain
  • cerebellum receives afferents from sensory areas and efferent copies of the plan from the cortex and calculates the movement

–> based on previous experiences it predicts the outcome of the plan and sends prediction error to the cortex for adjustment of the plan

40
Q

when grabbing an object, we somehow do not lose control over it, even when the weight, shape and characteristics of the objects are not exactly as predicted.
what is the role of the cerebellum in grip force control?

a. cerebellum receives pure afferent info from sensory areas and efferent info from the cortex, integrates the info and predicts the properties of the object to adjust the plan
b. cerebellum receives afferent info from sensory areas predicts the plan of action and send to the cortex, to execute the movement
c. sensory info is received by the thalamus and cortex, the cortex creates a plan for action, sends the plan to the cerebellum for prediction of the outcome of the plan
d. the cerebellum and cortex both act in parallel, to come up with an appropriate plan for action execution

A

a

41
Q

how can you test prism adaptation?

A

prism adaptation can be tested by throwing darts onto a target:
a. put on prism glasses (shift the vision off target) –> subjects throws darts at the target (but misses the target bc of the glasses)

b. repeat the action after learning that the target was off –> adjustment in x degrees
c. take the goggles off (no prism) –> throw the dart again –> although the prism is gone, subject throws dart the same way they did when they had the goggles on
d. patients with cerebellar lesions- no adaptation so subject keeps missing the target

42
Q

how can the ability of the cerebellum to learn and predict error be tested experimentally?

A
  • prism adaptation

- reach adaptation

43
Q

what can the reach adaptation task be used for? what is the procedure?

A
  • subject has to move the mouse on a screen to catch a target
  • with force applied on the manipulator the mouse will go elsewhere.
  • subject has to adapt and learn how much force is needed to move the mouse towards the target
  • in some trials, the force doesn’t change position of the mouse and subjects will still apply the force (bc they adapted to it in previous trials)
44
Q

what were the findings from the reach adaptation task in monkeys? which cerebellar cells are involved in learning?

A
  • when mouse isn’t on target anymore, climbing fibres (CF) from inferior olive send signal to PC which have many complex spikes.
  • at the same time, MF send input of simple spikes
  • -> when input from CF comes it modifies the synapse with MF, so LTD of MF-PC synapse occurs to generate prediction error based on input from CF.

–> the CF signal is a correcting signal –>LTD in MF-PC synapse, so the classical strong inhibition of cerebellar nuclei by PC is lower (more excitation).

45
Q

what is the principle of the visual threat eyebkink response (VTER). is this an acquired to a born ability?

A
  • A highly cerebellum response to visual cues.
  • If something flies into our eyes (but doesn’t touch), we close our eyes immediately because our brain registers it as a threat.
  • This is an acquired response- babies don’t blink in response to visual threat until they are ~3 months old.
46
Q

what circuits underlie conditioned eye blink?How could it be tested empirically?

A
  • conditioning task with a tone as CS paired with an airpuff as US.
  • use an airpuff as an error signal to the eye (airpuff–> bad–>response)

mechanism:
a. airpuff info is transferred to the cerebellum via climbing fibres (CF) in the inferior olive
b. (conditioned) tone is delivered via mossy fibres (MF)
c. tightly coupled CF and MF info coming to the cerebellum the same time leads to LTD in Purkinjee cells (PC) and parallel fibres (PF).
d. LTD of PC increases excitation of nuclei (less inhibition coming from PC)
=> RESPONSE

47
Q

according to the conditioned eye blink response model…(choose the WRONG answer)

a. signal from CF and MF depresses PC so they don’t inhibit cerebellar nuclei to the same extent
b. it is unclear how LTD in interneurons affects the resoonse
c. LTD occurs in all PC
d. it is unclear how interaction between learning systems (e.g. cerebellum and basal ganglia) contributes to the acquirement of the conditioned response
e. an unconditioned stimulus (airpuff) is paired with a conditioned stimulus (tone)

A

c

48
Q

what is the difference between the new and old views on cerebellar-cerebral connections

A

Old view:

  • reciprocal/efferent cerebello-cerebero connections go primarily to the primary motor cortex
  • the role of the cerebellum is mostly to improve motor function and not sensory/cognitive functions

New view:

  • there are reciprocal cerebello-cerebro connections not only with the motor areas but also with many other areas like cognitive cortical areas, premotor areas and parietal areas => cerebellum is involved in many functions other than motor
  • especially the lateral hemisphere projects to non-motor areas
49
Q

which of the following statements is/are correct?

a. lobule 6 (both left and right) is involved in speech generation
b. the left lateral hemisphere is involved in word association and generation
c. lobule 6 (both left and right) is involved in word association and generation
d. the right lateral hemisphere is involved in word generation and association
e. lobule 8A is involved in speech generation

A

a, d

50
Q

what are the symptoms of cerebellar cognitive affective syndrome?

A
  • disturbances of executive functions (planning, set shifting..)
  • impaired spatial cognition
  • “flattening” or “blunting” of personality
  • linguistic difficulties